sbcS sbcC null mutations allow RecF-mediated repair of arrested replication forks in rep recBC mutants

We have proposed previously that, in Escherichia coli, blockage of replicat ion forks can lead to the reversal of the fork. Annealing of the newly synt hesized strands creates a double-stranded end adjacent to a Holliday juncti on. The junction is migrated away from the DNA end by RuvAB and can be clea ved by RuvC, while RecBCD is required fear the repair of the double-strande d tail. Consequently, the rep mutant, in which replication arrests are freq uent and fork reversal occurs, requires RecBCD for growth. We show here tha t the combination of sbcB sbcCD null mutations restores the viability to re p recBC mutants by activation of the RecF pathway of recombination. This sh ows that the proteins belonging to the RecF pathway are able to process the DNA ends made by the replication fork reversal into a structure that allow s recombination-dependent replication restart. However, we confirm that, un like sbcB null mutations, sbcB15, which suppresses all other recBC mutant d efects, does not restore the viability of rep recBC sbcCD strains. Mle also show that ruvAB inactivation suppresses the lethality and the formation of double-stranded breaks (DSBs) in a rep recBC recF strain, totally deficien t for homologous recombination, as well as in rep recBC mutants. This confi rms that RuvAB processing of arrested replication forks is independent of t he presence of recombination intermediates.